Bahman Arrhythmia Clinic

The last decade has witnessed a growing consensus that pulmonary vein (PV) isolation is an essential endpoint of AF ablation. The Achilles' hill of such ablation is resumption of conduction through PV's (Gap's). The following case nicely demonstrates the importance of finding triggers inside PV's, isolation of PV and looking for evolution of gaps through the line of ablation.
     The patient was a 48 year old woman who was referred to us from Ghazvin City for ablation.  She had a history of very frequent episodes of palpitation due to both AT and AF. The symptoms were quite refractory to antiarrhythmic drugs. Cessation of flecainide 3 days before ablation leaded to an incessant AT with a ventricular rate of about 160-180 bpm (fig.1). The patient was brought to EP lab and diagnostic catheters were placed in RV, RA, His and coronary sinus. We noticed an AT with cycle length of 220-240 msec which was alternatively converted to AF(fig.2). With respect to P wave morphology and pattern of intracardiac electrical activation and behavior of the arrhythmia, the origin of AT was assumed to be inside PV's.

                    Figure 1: 12 lead electrogram during AT

                                       figure 2: intracardiac tracing revealing degeneration of AT to AF
                                       (catheter of ablation inside RUPV showing the earliest potential)

So after septostomy, a multielectrode catheter (lasso) was placed alternatively inside each PV. Recordings inside right upper PV (RUPV) (fig.3) revealed the earliest potential during stable AT inside this vessel. Focal ablation based on activation mapping inside RUPV failed to abolish the arrhythmia; So isolation of right PV's was planned to inhibit the conduction of AT from PV to LA.

Figure 3: Catheter of Lasso inside RUPV                                     Venogram of RUPV

Based on geometry of LA and PV's constructed by Navx system ,we began to create circular ablation line  by point by point RF application from above the RUPV anteriorly downward to the bottom of right lower PV (RLPV) and then upward poteriorly to the start point to encircle both right PV's. (The linear ablation between two PV's may be associated with PV stenosis,  so instead of isolation of just RUPV, isolation of both veins through the antrum was performed). During ablation, the catheter was kept as far as possible away from PV ostium to avoid PV stenosis; RF burn at each point was not allowed to prolong more than 15-20 seconds in fear of perforation and tamponade. [This is the cutting edge of AF ablation; the more effective burn in the thin muscle of LA is associated with more perforation and less powerful burns are associated with more gaps and more recurrences]

    During the last RF applications before completion of the line, signs of isolation appeared. The patient's rhythm which had become sustained irregular AF converted to stable AT (fig.4) and by each burn the rate of AT decreased more and more (despite high rate activity inside RUPV).

                        figure 4: Conversion of AF to AT during last RF burns around PV's

    Finally the last RF application suddenly converted the slow AT to sinus rhythm and none of PV potentials were conducted to the atria(the door was closed) (fig.5). It's really a great moment to notice AF or AT inside PV but sinus rhythm in atria (like watchig a lion through a cage). It nicely reveals the proposed mechanism of AF which was first brought into practice by Haïssaguerre  a decade ago (although by focal ablation).

    

                            figure 5: Termination of slow AT following the last RF application

     However, happiness may not last for a long time as some regions in the ablation line begin to heal and reconnect PV with atrium (GAP's). Anticipating this issue, we left the patient for 20 minutes (break for tea!). Coming back to the patient, we found an ectopic rhythm with a rate of about 90 bpm. Although slow but it was not sinus and the pattern of intracardiac activation of the atria was exactly the same as the preexisted arrhythmia (fig.6). Yes! The gaps were evolving and allowed some of PV potentials conducting into atrium. This conduction although was accompanied with block, however complete healing of these incompletely injured tissues and unblocked conduction would result in recurrence of AF in near future.

      figure 6: conduction of PV potentials with block through the gap generating a slow AT

      So we looked carefully for gaps along the ablated line by finding foci with preserved potentials and capability of being captured by pacing (it means alive!). Focal ablation at 3-4 such lived points eventually resulted in achieving sinus rhythm. After waiting for another 30 minutes (another cup of tea!) fortunately there was no gap and the work was done. She was discharged the day after and during the last month she has been entirely asymptomatic with no antiarrhythmic drug.

The interesting case presented, clearly demonstrates two fundamental practical issues in AF ablation. The first one is the major role of triggers in AF. Although triggers inside PV's account for more than 90 percent of episodes of paroxysmal AF, however looking for such triggers as target before ablation absolutely yields better results than blindly isolating PV's at both sides. Although infrequent, however there are many reports of AF triggers at other regions such as SVC and other parts. Even a simple AVNRT can be degenerated spontaneously to AF and in a patient with inducible AVNRT , slow pathway modification could prevent AF episodes while a complex bilateral PV isolation could be quite ineffective. So a complete study especially arrhythmia induction (for finding triggers) seems to be an essential part of a successful ablation for AF. In our case, runs of AT originating from RUPV degenerating to AF were evident and isolation of these triggers completely terminated both AT and AF, so there was no need for left PV's isolation because the goal was arrhythmia not PV's.

 

The second point in this case is the importance of gaps. Gaps are the leading cause of recurrences which are reported to occur after about 30 percent of ablations performed for paroxysmal ones. As mentioned before, the relatively low energy and short time RF applications (to avoid perforation) leads to less efficient burns and less injury. So transmural scar may not be created at some points along the ablation line.  These gaps which are capable of electrical conduction reconnect PV with LA and eventually AF recurs. The least work we could do in this case was to wait for early gap formation. However we could not do any thing if other gaps would appear in the next 6 hours or more. It's possible that in early future other sources of energy or methods will solve the problem of gaps.

 

 

 

Ali Kharazi M.D.

        Mohammad Alasti M.D.